抗人 SIRT3 抗体对
01AB03392
Sirtuin 3 (SIRT3) is the primary NAD+-dependent deacetylase localized within the mitochondrial matrix, where it serves as a master regulator of metabolic fidelity and energy homeostasis. It features a conserved enzymatic core with a Rossmann fold that enables the deacetylation of diverse substrates involved in fatty acid oxidation, the TCA cycle, and the electron transport chain. Key partners include ACADM, OGDH, and GLUD1, as well as antioxidant enzymes like MnSOD2. By enhancing ATP production and mitochondrial biogenesis via PGC-1alpha, SIRT3 protects against oxidative stress and inhibits the opening of the mitochondrial permeability transition pore. Clinically, SIRT3 deficiency is linked to insulin resistance in skeletal muscle, cardiac hypertrophy, and acute kidney injury. Its ability to deacetylate FOXO3alpha and GSK3beta further supports its role in tissue protection, making it a critical target for research into metabolic and age-related diseases.
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技术参数
- 靶点基因名
- SIRT3
- 基因别名
- SIR2L3
- 蛋白别名
- sirtuin 3; SIRT3
- UniProt
- Q9NTG7
- 物种
- Human
产品详情
- 靶点名称
- SIRT3
- 蛋白名称
- sirtuin 3
- 蛋白别名
- NAD-dependent protein deacetylase sirtuin-3; mitochondrial; hSIRT3; NAD-dependent protein delactylase sirtuin-3; Regulatory protein SIR2 homolog 3; SIR2-like protein 3
- 靶点基因名
- SIRT3
- 基因别名
- SIR2L3
- UniProt
- Q9NTG7
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
Sirtuin 3 (SIRT3) is the primary NAD+-dependent deacetylase localized within the mitochondrial matrix, where it serves as a master regulator of metabolic fidelity and energy homeostasis. It features a conserved enzymatic core with a Rossmann fold that enables the deacetylation of diverse substrates involved in fatty acid oxidation, the TCA cycle, and the electron transport chain. Key partners include ACADM, OGDH, and GLUD1, as well as antioxidant enzymes like MnSOD2. By enhancing ATP production and mitochondrial biogenesis via PGC-1alpha, SIRT3 protects against oxidative stress and inhibits the opening of the mitochondrial permeability transition pore. Clinically, SIRT3 deficiency is linked to insulin resistance in skeletal muscle, cardiac hypertrophy, and acute kidney injury. Its ability to deacetylate FOXO3alpha and GSK3beta further supports its role in tissue protection, making it a critical target for research into metabolic and age-related diseases.